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Roke. J Cereb Blood Flow Metab 27:1684691. https://doi.org/10.1038/sj.jcbfm.9600475 99. Zlokovic BV (2008) The blood-brain barrier in wellness and chronic neurodegenerative disorders. Neuron 57:17801. https://doi.org/10.1016/j. neuron.2008.01.
den Haan et al. Acta Neuropathologica Communications (2018) 6:75 https://doi.org/10.1186/s40478-018-0577-RESEARCHOpen AccessDifferent curcumin types selectively bind fibrillar amyloid beta in post mortem Alzheimer’s disease brains: Implications for in-vivo Recombinant?Proteins KPNB1 Protein diagnosticsJurre den Haan1* , Tjado H. J. Morrema2, Annemieke J. Rozemuller2, Femke H. Bouwman1 and Jeroen J. M. HoozemansAbstractThe combined fluorescent and A-binding properties from the dietary spice curcumin could yield diagnostic objective within the search for a non-invasive A-biomarker for Alzheimer’s disease (AD). Having said that, proof on the binding properties of curcumin, its conjugates and clinically utilised bio-available formulations to AD neuropathological hallmarks is scarce. We thus assessed the binding properties of various curcumin types to various neuropathological deposits in post-mortem brain tissue of situations with AD, other neurodegenerative diseases, and controls. Post mortem brain tissue was histochemically assessed for the binding of curcumin, its isoforms, conjugates and bio-available types and compared to routinely utilized staining techniques. For this study we integrated brains of early onset AD, late onset AD, main age-related tauopathy (Portion), cerebral amyloid angiopathy (CAA), frontotemporal lobar degeneration (FTLD) with tau or TAR DNA-binding protein 43 (TDP-43) inclusions, dementia with Lewy bodies (DLB), Parkinson’s disease (PD) and manage circumstances with no brain pathology. We located that curcumin binds to fibrillar amyloid beta (A) in plaques and CAA. It does not particularly bind to inclusions of protein aggregates in FTLD-tau circumstances, TDP-43, or Lewy bodies. Curcumin isoforms, conjugates and bio-available types show affinity for the exact same A structures. Curcumin staining overlaps with immunohistochemical detection of A in fibrillar plaques and CAA, and to a lesser extent cored plaques. A weak staining of neurofibrillary tangles was observed, whilst other structures immunopositive for phosphorylated tau remained negative. In conclusion, curcumin, its isoforms, conjugates and bio-available types selectively bind fibrillar A in plaques and CAA in post mortem AD brain tissue. Curcumin, getting a food additive with fluorescent properties, is for that reason an exciting candidate for in-vivo diagnostics in AD, for example in retinal fluorescent imaging. Keyword phrases: Curcumin, Amyloid-beta, Alzheimer’s disease, Cerebral amyloid angiopathy (CAA), Neurodegeneration, Biomarker, ImmunohistochemistryIntroduction Aggregation and extracellular deposition in the amyloidbeta (A) peptide in amyloid plaques is actually a pathological hallmark and an early event within the pathophysiology of Alzheimer’s disease (AD) [4, 18]. Presently AD diagnosis could be created with assist of clinical criteria with the* Correspondence: [email protected] 1 Department of Neurology, Amsterdam Neuroscience, VU University Healthcare Center Alzheimer Center, Mailbox 7057, 1007, MB, Amsterdam, the Netherlands Full list of author details is Recombinant?Proteins CD73/5′-Nucleotidase Protein accessible in the end of your articlesupport of measurements of A12 and tau- 181 in cerebrospinal fluid (CSF), amyloid-positron emission tomography (PET), cortical atrophy on magnetic resonance imaging (MRI), or hypo-metabolism by fluorodeoxyglucose ET (FDG-PET) [3.

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